Making Computer Chips With Human Cells

In 2030 the smartphones could contain a super powerful processor that perform a quintillon operations per second, a thousand times faster than smartphone biologicalmodels in 2020. This huge performance gains is possible because a new biological chip using lab-grown human neurons,  better than silicon chips, can change their internal structure, adapting to a user’s usage pattern and leading to huge gains in efficiency.

In December 2021, Melbourne-based Cortical Labs grew groups of neurons (brain cells) that were incorporated into a computer chip. The resulting hybrid chip works because both brains and neurons share a common language: electricity.

In silicon computers, electrical signals travel along metal wires that link different components together. In brains, neurons communicate with each other using electric signals across synapses (junctions between nerve cells). In Cortical LabsDishbrain system, neurons are grown on silicon chips. These neurons act like the wires in the system, connecting different components. The major advantage of this approach is that the neurons can change their shape, grow, replicate, or die in response to the demands of the system.

Dishbrain could learn to play the arcade game Pong faster than conventional AI systems. The developers of Dishbrain said: “Nothing like this has ever existed before … It is an entirely new mode of being. A fusion of silicon and neuron.”

Cortical Labs believes its hybrid chips could be the key to the kinds of complex reasoning that today’s computers and AI cannot produce. Another start-up making computers from lab-grown neuronsKoniku, believes their technology will revolutionise several industries including agriculture, healthcare, military technology and airport security. Other types of organic computers are also in the early stages of development.

While silicon computers transformed society, they are still outmatched by the brains of most animals. For example, a  more data storage than an average iPad and can use this information a million times faster. The human brain, with its trillion neural connections, is capable of making 15 quintillion operations per second.

Source: https://theconversation.com/

Viagra Users Are 69% Less Likely to Develop Alzheimer’s

Viagra could be a useful treatment against Alzheimer’s disease, according to a US study. Alzheimer’s disease, the most common form of age-related dementia, affects hundreds of millions of people worldwide. Despite mounting numbers of cases, however, there is currently no effective treatment.

Using a large gene-mapping network, researchers at the Cleveland Clinic integrated genetic and other data to determine which of more than 1,600 Food and Drug Administration-approved drugs could be an effective treatment for Alzheimer’s disease. They gave higher scores to drugs that target both amyloid and tau – two hallmarks of Alzheimer’s – compared with drugs that targeted just one or the other.

US scientists say users of sildenafil – the generic name for Viagra – are 69% less likely to develop the form of dementia than non-users

“Sildenafil, which has been shown to significantly improve cognition and memory in preclinical models, presented as the best drug candidate,” said Dr Feixiong Cheng, the study lead.

Researchers then used a database of claims from more than 7 million people in the US to examine the relationship between sildenafil and Alzheimer’s disease outcomes by comparing sildenafil users to non-users.

They found sildenafil users were 69% less likely to develop Alzheimer’s disease than non-sildenafil users after six years of follow-up. To further explore the drug’s potential effect on Alzheimer’s disease, researchers developed a lab model that showed that sildenafil increased brain cell growth and targeted tau proteins, offering insights into how it might influence disease-related brain changes. Cheng cautioned that the study does not demonstrate a causal relationship between sildenafil and Alzhemer’s disease. Randomised clinical trials involving both sexes with a placebo control were needed to determine sildenafil’s efficacy, he said.

Dr Ivan Koychev, a senior clinical researcher at the University of Oxford, who was not involved in the study, said it was “an exciting development” because “it points to a specific drug which may offer a new approach to treating the condition”.

Prof Tara Spires-Jones, deputy director of the Centre for Discovery Brain Sciences at the University of Edinburgh, said there were several important limitations to consider. “While these data are interesting scientifically, based on this study, I would not rush out to start taking sildenafil as a prevention for Alzheimer’s disease.”

Dr Susan Kohlhaas, director of research at Alzheimer’s Research UK, said: “Being able to repurpose a drug already licensed for other health conditions could help speed up the drug discovery process and bring about life-changing dementia treatments sooner. “Importantly, this research doesn’t prove that sildenafil is responsible for reducing dementia risk, or that it slows or stops the disease. The only way to test this would be in a large-scale clinical trial measuring sildenafil effect against the usual standard of care.”

The findings were published in Nature Aging.

Source: https://www.theguardian.com/

Eyes Provide Peek at Alzheimer’s Disease Risk

Protein deposits in retina and brain appear to parallel possible neurodegeneration, an insight that might lead to easier, quicker detection. Amyloid plaques are protein deposits that collect between brain cells, hindering function and eventually leading to neuronal death. They are considered a hallmark of Alzheimer’s disease (AD), and the focus of multiple investigations designed to reduce or prevent their formation, including the nationwide A4 study.

But amyloid deposits may also occur in the retina of the eye, often in patients clinically diagnosed with AD, suggesting similar pathologies in both organs. In a small, cross-sectional study, a team of researchers, led by scientists at University of California San Diego School of Medicine, compared tests of retinal and brain amyloids in patients from the A4 study and another study (Longitudinal Evaluation of Amyloid Risk and Neurodegeneration) assessing neurodegeneration risk in persons with low levels of amyloid.

Like the proverbial “windows to the soul,” the researchers observed that the presence of retinal spots in the eyes correlated with brain scans showing higher levels of cerebral amyloid. The finding suggests that non-invasive retinal imaging may be useful as a biomarker for detecting early-stage AD risk.

Amyloid deposits tagged by curcumin fluoresce in a retinal scan.

This was a small initial dataset from the screening visit. It involved eight patients,” said senior author Robert Rissman, PhD, professor of neurosciences at UC San Diego School of Medicine. “But these findings are encouraging because they suggest it may be possible to determine the onset, spread and morphology of AD — a preclinical diagnosis — using retinal imaging, rather than more difficult and costly brain scans. We look forward to seeing the results of additional timepoint retinal scans and the impact of solanezumab (a monoclonal antibody) on retinal imaging. Unfortunately we will need to wait to see and analyze these data when the A4 trial is completed.”

The findings published in the journal Alzheimer’s & Dementia.

https://ucsdnews.ucsd.edu/